ReviewFrontiers in immunology2025
From chronic inflammation to immune escape: mapping the tumor microenvironment evolution in renal cell carcinoma.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Immune Checkpoint Inhibitor-Related Pneumonitis in Renal Cell Carcinoma: Clinical Features, Mechanisms, and Lessons from Lung Cancer.Biomolecules · 2026Review
- Review
- Feasibility and Safety of a Ketogenic Diet During Systemic Therapy for Metastatic Renal Cell Carcinoma: Results from the Cetorein Pilot Study.Nutrients · 2026Article
- Imaging of synchronous multifocal renal masses: a case report.Frontiers in medicine · 2026Article
- Immune-excluded and immune-suppressive tumor microenvironments: mechanisms, spatial biomarkers, and therapeutic rewiring.Frontiers in oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal cell carcinoma (RCC) evolves within a chronic inflammatory renal niche, where angiogenesis, metabolism, and immune programs synergize to reshape the tumor immune microenvironment (TIME). Recurrent renal damage and tissue hypoxia sustain NF-κB/STAT3 and HIF-VEGF signaling, while a sustained IFN-γ response enhances antigen presentation while inducing inhibitory checkpoints, promoting a state of "inflammation but constrained." Single-cell and spatial studies reveal early microenvironment heterogeneity and the chemokine-checkpoint paradox: regions enriched in CXCL9/10 coexist with endothelial inertia, cancer-associated fibroblasts (CAFs)-mediated stromal barriers, and metabolic stress, which collectively exclude functional CD8
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.